Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The neurological features of acromegaly are reviewed and two cases are reported. The most common neurological complications of active hypersomatotropism are headache, acroparesthesia and visual disturbance. Primary peripheral neuropathy, myopathy, entrapment myelopathy and/or cauda equina syndrome are uncommon, especially in young acromegalics. It is postulated that peripheral neuropathy in acromegaly is due to the entrapment of a nerve secondary to a soft tissue edematous mechanism by traumatic compression, angulation and/or stretching of the nerve in acquired extraspinal intermuscular, fibrous or osseofibrous tunnel stenosis; and/or in acquired spinal lateral recess stenosis, rather than true primary neuropathic or secondary endocrinological complications of hypersomatotropism. Proximal weakness is more likely arthropathic rather than myopathic, neuropathic or endocrinologic. Differential diagnosis of backache is briefly discussed. Further investigations of the mechanisms and the conservative treatment for neurological involvements in acromegaly are needed.
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PMID:Neurological features of acromegaly: a review and report of two cases. 284 43

Ergotamine tartrate (ET) and dihydroergotamine mesylate (DHE) have been widely and effectively used in the treatment of migraine for many decades, although few randomized, controlled clinical trials have been conducted with these compounds. To compare their safety profiles, the world literature on the two agents was surveyed. The results are summarized, along with a critical analysis of the strengths and limitations of the various sources of safety data (in vitro research, animal studies, Phase I and II studies, controlled clinical trials, and postmarketing surveillance). Significant pharmacologic and safety differences exist between ET and DHE. Dihydroergotamine mesylate is a less potent arterial vasoconstrictor than ET, although nearly equipotent as a venoconstrictor. It is a more potent alpha-adrenergic antagonist, but is much less emetic, has less effect on the uterus, and is not associated with rebound headache. Adverse effects associated with ET (which are often due to excessive dosage and/or chronic usage) include nausea, acroparesthesia, ischemia, habituation and overuse headache, and, rarely, overt ergotism. Reports of serious adverse effects following recommended doses of DHE are rare. As with most antimigraine drugs, the most frequent adverse effect with intravenous (i.v.) DHE is nausea; however, following intramuscular (i.m.) or intranasal (IN) administration, the incidence of nausea is low and concomitant administration of an antiemetic is not needed. In patients without contraindications, both DHE and ET are safe and effective when used in recommended doses. Nearly 50 years of clinical experience without major safety problems allows a high level of confidence in their clinical use.
Headache 1997
PMID:Ergotamine tartrate and dihydroergotamine mesylate: safety profiles. 900 72

Fabry Disease (FD) is an X-linked lysosomal storage disorder (prevalence about 1 : 100 000) caused by a genetic defect associated with a lack of alpha-galactosidase A (alpha-GAL) enzyme activity. As a consequence, neutral glycosphingolipides can not be cleaved and metabolized, and accumulate in lysosomes of several tissues, particularly in vascular endothelium and smooth muscle cells. The most prominent symptoms comprise pain attacks and acroparesthesia, angiokeratoma, corneal opacity, renal and cardiac dysfunction, hypo- and anhidrosis, gastrointestinal symptoms, and cerebrovascular dysfunction with vertigo, headache, and cerebral ischemia. Characteristic symptoms of FD can occur in male and female patients with the same prevalence, while females with FD seem to be less severely affected. The course of untreated illness is progressive with considerable interindividual variability. Since 2001 two enzyme replacement therapies are approved which can possibly stop the disease progress and alleviate symptoms. The very few reports and clinical observations have shown that a very high proportion of FD patients develop neuropsychiatric symptoms. However, accurate data are lacking. Although the pathophysiologic mechanisms are quite unknown, it is surmised that sphingolipid deposits in the endothelium of small cerebral vessels lead to regional cerebral ischemia accompanied by neuropsychiatric symptoms and deficits. Furthermore, patients with FD are chronically distressed by pain attacks and additional somatic and psychological impairment. Frequently, pain attacks are triggered by psychosocial stress. The high interindividual variability can, thus, also be interpreted on the basis of existing stress and coping models. The present paper will review the presently available psychiatric and neuropsychological findings in FD and will discuss difficulties associated with classification and differential diagnosis of psychiatric disorders occurring in patients with FD.
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PMID:[Psychiatric and neuropsychological signs and symptoms in patients with fabry disease: literature review]. 1628 13